The involvement of miR-23a/APAF1 regulation axis in colorectal cancer.

Int J Mol Sci

Department of Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.

Published: July 2014

AI Article Synopsis

  • Recent research suggests microRNAs (miRNAs) could serve as important biomarkers in cancer, with this study focusing on miR-23a's role in colorectal cancer (CRC) development.
  • Experiments showed that inhibiting miR-23a in CRC cell lines increased cell death and reduced cell survival, indicating its potential role in apoptosis resistance.
  • The study also found an inverse relationship between miR-23a and APAF1 expression, proposing that targeting the miR-23a/APAF1 pathway could be useful for cancer treatment and prognosis.

Article Abstract

Recent advances in microRNAome have made microRNAs (miRNAs) a compelling novel class of biomarker in cancer biology. In the present study, the role of miR-23a in the carcinogenesis of colorectal cancer (CRC) was investigated. Cell viability, apoptosis, and caspase 3/7 activation analyses were conducted to determine the potentiality of apoptosis resistance function of miR-23a in CRC. Luciferase assay was performed to verify a putative target site of miR-23a in the 3'-UTR of apoptosis protease activating factor 1 (APAF1) mRNA. The expression levels of miR-23a and APAF1 in CRC cell lines (SW480 and SW620) and clinical samples were assessed using reverse transcription-quantitative real-time PCR (RT-qPCR) and Western blot. We found that the inhibition of miR-23a in SW480 and SW620 cell lines resulted in significant reduction of cell viability and promotion of cell apoptosis. Moreover, miR-23a up-regulation was coupled with APAF1 down-regulation in CRC tissue samples. Taken together, miR-23a was identified to regulate apoptosis in CRC. Our study highlights the potential application of miR-23a/APAF1 regulation axis in miRNA-based therapy and prognostication.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4139809PMC
http://dx.doi.org/10.3390/ijms150711713DOI Listing

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